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Background: There is inconsistent evidence about the association between inflammatory disorders with depression and anxiety onset in a primary care context. The study aimed evaluate the risk of depression and anxiety within multisystem and organ-specific inflammatory disorders. Methods: Prospective cohort study with primary care patients from the UK Clinical Practice Research Datalink diagnosed with an inflammatory disorder between 1st of January 2001 and 31st of December 2016. These patients were matched on age, gender, practice, and index date with patients without an inflammatory disorder. The study exposures were seven chronic inflammatory disorders. Clinical diagnosis of depression and anxiety represented the outcome measures of interest. Findings: Among 538,707 participants, the incidence of depression ranged from 14 per 1000 person-years (severe psoriasis) to 9 per 1000 person-years (systemic vasculitis), substantively higher compared to their comparison group (5 to 7 per 1000 person-years). Hazard ratios (HR) of multiple depression and anxiety events were 16% higher within inflammatory disorders (HR, 1·16, 95%CI 1·12-1·21, p

Older adults often complain about their memory ability, but it is not clear to what extent subjective memory complaints accurately reflect objective cognitive dysfunctions. The concordance between objective and subjective cognitive performance may be affected by depressive symptoms and by declining insight into cognitive deficits. This study aims to examine longitudinal associations between subjective memory complaints, objective cognitive performance and depressive symptoms. 11,092 participants aged 50 years and above from the English Longitudinal Study of Ageing were followed-up every 2 years over a 6-year period. Two processes latent growth curve models (LGCM) examined associations between levels and changes in several cognitive abilities and subjective memory complaints, unadjusted for depression symptoms. Then three processes LGCM examined associations between levels and changes in depressive symptoms, subjective memory complaints and objective cognitive abilities in the overall sample, and separately among persons with mild cognitive impairment at baseline. More subjective memory complaints were associated with poorer performance in all cognitive domains at baseline. Steeper decline in immediate recall, verbal fluency and processing speed performance was associated increasing subjective memory complaints both in the overall sample and among persons with mild cognitive impairment. Increasing depressive symptoms were associated with both objective and subjective cognitive decline in the overall sample, and only with subjective memory decline among cognitively impaired persons. Self-reported memory complaints may have the potential to identify decline in objective cognitive performance that cannot be explained by depressive symptoms. Among cognitively impaired persons depressive symptoms may amplify subjective but not objective cognitive decline.

Importance The emerging paradigm of treat-to-target in psoriasis requires accurate monitoring of treatment response. The commonly used physician global assessment tool does not capture the patient’s perception of their disease. Patient assessments facilitate shared decision-making and foster patient-centered care; however, recent research reports a discordance between patient- and physician-reported psoriasis severity. Understanding the factors underlying this discordance may improve treatment satisfaction and disease outcomes. Objectives To evaluate the discordance between patient- and physician-reported measures of psoriasis severity and assess the association with patient mental health status. Design, Setting, and Participants A cohort study using repeated cross-sectional analysis of real-world longitudinal data was conducted at a large specialist psoriasis service serving London and Southeast England. A total of 502 patients attending the psoriasis service between May 12, 2016, and November 1, 2018, were included. Data analysis was conducted July 22 to October 22, 2019. Main Outcomes and Measures Psoriasis severity was assessed on each visit with identical 5-point physician and patient global assessment scales (clear/nearly clear, mild, moderate, severe, and very severe). Each patient completed validated self-report screens for depression and anxiety on each visit. Results Longitudinal data from 502 individuals with psoriasis (1985 total observations) were available. A total of 339 patients (68%) were men, 396 (79%) were White, mean (SD) age was 47 (13) years, and 197 patients (39%) had concurrent psoriatic arthritis, 43 (9%) screened positive for depression, and 49 (10%) screened positive for anxiety. There was discordance between physician and patient measures of disease severity in 768 of 1985 office appointments (39%); on 511 visits (26%) patients rated their psoriasis as less severe and on 257 visits (13%) patients rated their psoriasis as more severe compared with their physician. Individuals who screened positive for depression or anxiety were more likely to overestimate their psoriasis severity compared with their physician (relative risk ratio: depression, 2.7; 95% CI, 1.6-4.5; anxiety, 2.1; 95% CI, 1.3-3.4). These findings remained statistically significant after adjustment for age, ethnicity, sex, body mass index, smoking, number of comorbidities, treatment modality, and presence of psoriatic arthritis. Conclusions and Relevance The findings of this cohort study suggest that discordance between patient and physician assessments of psoriasis severity is associated with patients’ mental health status. Recognition of anxiety and depression in individuals with psoriasis appears to be important when interpreting patient-reported outcome measures and informing appropriate treatment decisions.

Background Anxiety and depression are common, debilitating and costly. These disorders are influenced by multiple risk factors, from genes to psychological vulnerabilities and environmental stressors, but research is hampered by a lack of sufficiently large comprehensive studies. We are recruiting 40,000 individuals with lifetime depression or anxiety and broad assessment of risks to facilitate future research. Methods The Genetic Links to Anxiety and Depression (GLAD) Study (www.gladstudy.org.uk) recruits individuals with depression or anxiety into the NIHR Mental Health BioResource. Participants invited to join the study (via media campaigns) provide demographic, environmental and genetic data, and consent for medical record linkage and recontact. Results Online recruitment was effective; 42,531 participants consented and 27,776 completed the questionnaire by end of July 2019. Participants’ questionnaire data identified very high rates of recurrent depression, severe anxiety, and comorbidity. Participants reported high rates of treatment receipt. The age profile of the sample is biased toward young adults, with higher recruitment of females and the more educated, especially at younger ages. Discussion This paper describes the study methodology and descriptive data for GLAD, which represents a large, recontactable resource that will enable future research into risks, outcomes, and treatment for anxiety and depression., Highlights • Online recruitment of 40,000 individuals with lifetime depression or anxiety. • Detailed online phenotyping combined with genetic and clinical data. • The study sample is severe, highly comorbid, with chronic psychopathology. • The study protocol enables recall of participants for future research and trials.

BackgroundCognitive impairment and depression often co-occur in older adults, but it is not clear whether depression is a risk factor for cognitive decline, a psychological reaction to cognitive decline, or whether changes in depressive symptoms correlate with changes in cognitive performance over time. The co-morbid manifestation of depression and cognitive impairment may reflect either a causal effect or a common cause, depending on the specific symptoms experienced and the cognitive functions affected.MethodThe study sample comprised 1506 community-dwelling older adults aged ⩾65 years from the Longitudinal Aging Study Amsterdam (LASA). We conducted cross-domain latent growth curve analyses to examine longitudinal associations between late-life depression dimensions (i.e. depressed affect, positive affect, and somatic symptoms) and specific domains of cognitive functioning (i.e. processing speed, inductive reasoning, immediate recall, and delayed recall).ResultsPoorer delayed recall performance at baseline predicted a steeper increase in depressed affect over time. Steeper decline in processing speed correlated with a steeper increase in somatic symptoms of depression over time.ConclusionsOur findings suggest a prospective association between memory function and depressed affect, whereby older adults may experience an increase in depressed affect in reaction to poor memory function. Somatic symptoms of depression increased concurrently with declining processing speed, which may reflect common neurodegenerative processes. Our findings do not support the hypothesis that depression symptoms may be a risk factor for cognitive decline in the general population. These findings have potential implications for the treatment of late-life depression and for the prognosis of cognitive outcomes.

ObjectivesFor many research cohorts, it is not practical to provide a “gold‐standard” mental health diagnosis. It is therefore important for mental health research that potential alternative measures for ascertaining mental disorder status are understood.MethodsData from UK Biobank in those participants who had completed the online Mental Health Questionnaire (n = 157,363) were used to compare the classification of mental disorder by four methods: symptom‐based outcome (self‐complete based on diagnostic interviews), self‐reported diagnosis, hospital data linkage, and self‐report medication.ResultsParticipants self‐reporting any psychiatric diagnosis had elevated risk of any symptom‐based outcome. Cohen's κ between self‐reported diagnosis and symptom‐based outcome was 0.46 for depression, 0.28 for bipolar affective disorder, and 0.24 for anxiety. There were small numbers of participants uniquely identified by hospital data linkage and medication.ConclusionOur results confirm that ascertainment of mental disorder diagnosis in large cohorts such as UK Biobank is complex. There may not be one method of classification that is right for all circumstances, but an informed and transparent use of outcome measure(s) to suit each research question will maximise the potential of UK Biobank and other resources for mental health research.

BackgroundDepression is a heterogeneous disorder with multiple aetiological pathways and multiple therapeutic targets. This study aims to determine whether atypical depression (AD) characterized by reversed neurovegetative symptoms is associated with a more pernicious course and a different sociodemographic, lifestyle, and comorbidity profile than nonatypical depression (nonAD).MethodsAmong 157 366 adults who completed the UK Biobank Mental Health Questionnaire (MHQ), N = 37 434 (24%) met the DSM-5 criteria for probable lifetime major depressive disorder (MDD) based on the Composite International Diagnostic Interview Short Form. Participants reporting both hypersomnia and weight gain were classified as AD cases (N = 2305), and the others as nonAD cases (N = 35 129). Logistic regression analyses were conducted to examine differences between AD and nonAD in depression features, sociodemographic and lifestyle factors, lifetime adversities, psychiatric and physical comorbidities.ResultsPersons with AD experienced an earlier age of depression onset, longer, more severe and recurrent episodes, and higher help-seeking rates than nonAD persons. AD was associated with female gender, unhealthy behaviours (smoking, social isolation, low physical activity), more lifetime deprivation and adversity, higher rates of comorbid psychiatric disorders, obesity, cardiovascular disease (CVD), and metabolic syndrome. Sensitivity analyses comparing AD persons with those having typical neurovegetative symptoms (hyposomnia and weight loss) revealed similar results.ConclusionsThese findings highlight the clinical and public health significance of AD as a chronic form of depression, associated with high comorbidity and lifetime adversity. Our findings have implications for predicting depression course and comorbidities, guiding research on aetiological mechanisms, planning service use and informing therapeutic approaches.

Background and objectives Research indicates that individuals at-risk for depression are characterized by high sensitivity to loss and reduced sensitivity to reward. Moreover, it has been shown that attentional bias plays an important role in depression vulnerability. The current study aimed to examine the interplay between these risk factors for depression by examining the development of attentional bias toward reward and loss signals in dysphoric participants (individuals with elevated levels of depressive symptoms). Methods Shapes were conditioned to reward and loss and subsequently presented in a dot probe task in a sample of dysphoric and nondysphoric participants. Results Nondysphoric individuals oriented towards reward-related signals whereas dysphoric individuals failed to develop a reward-related attentional bias. This attentional effect was observed in the absence of group differences in motivational factors. No group differences were found for attentional bias for loss-related signals, despite the fact that dysphoric individuals performed worse in response to losing. Limitations The current sample is not clinical thus generalization to clinical depression is not warranted. Conclusions We argue that impaired early attentional processing of rewards are an important cognitive risk factor for anhedonic symptoms in persons with dysphoria.

Objectives: This study aims to examine cohort differences in cognitive performance and rates of change in episodic memory, processing speed, inductive reasoning, and general cognitive performance and to investigate whether these cohort effects may be accounted for by education attainment. Method: The first cohort (N = 705) was born between 1920 and 1930, whereas the second cohort (N = 646) was born between 1931 and 1941. Both birth cohorts were aged 65 to 75 years at baseline and were followed up 3 and 6 years later. Data were analyzed using linear mixed models. Results: The later born cohort had better general cognitive performance, inductive reasoning, and processing speed at baseline, but cohort differences in inductive reasoning and general cognitive performance disappeared after adjusting for education. The later born cohort showed steeper decline in processing speed. Memory decline was steeper in the earlier born cohort but only from Time 1 to Time 3 when the same memory test was administered. Education did not account for cohort differences in cognitive decline. Discussion: The later born cohort showed better initial performance in certain cognitive abilities, but no better preservation of cognitive abilities overtime compared with the earlier born cohort. These findings carry implications for healthy cognitive aging.